First Report of Pseudomonas syringae pv. aptata Causing Bacterial Leaf Spot on Sugar Beet in Serbia.

A severe bacterial leaf spot was observed during June and July 2013 on commercial cultivars of sugar beet (Beta vulgaris var. saccharifera) in the Vojvodina Province of Serbia. Serbia is a major sugar beet production area in southeastern Europe, with 62,895 ha and 3 million tons of sugar beet yield in 2013. A foliar leaf spot observed in 25 commercial sugar beet fields surveyed ranged from 0.1 to 40% severity. Symptoms were characterized as circular or irregular, 5- to 20-mm diameter, white to light brown necrotic spots, each with a dark margin. Diseased leaves were rinsed in sterilized, distilled water (SDW) and dried at room temperature, and leaf sections taken from the margin of necrotic tissue were macerated in SDW. Isolations from 48 symptomatic leaves onto nutrient agar with 5% (w/v) sucrose (NAS) produced bacterial colonies that were whitish, circular, dome-shaped, and Levan-positive. Representative isolates (n = 105) were Gram negative; aerobic; positive for catalase, fluorescence on King's medium B, and tobacco hypersensitivity; and negative for oxidase, potato rot, and arginine dehydrolase. These reactions corresponded to LOPAT group Ia, which includes Pseudomonas syringae pathovars (2). Repetitive extragenic palindromic sequence (rep)-PCR was used for genetic fingerprinting the isolates using the REP, ERIC, and BOX primers. Twenty-five different profiles were obtained among the strains. From each profile group, one representative strain was sequenced for the gyrB gene (1). Four heterogenic groups were observed, and representative gyrB gene sequences of each group were deposited in the NCBI GenBank (Accession Nos. KJ950024 to KJ950027). The sequences were compared with those of pathotype strain P. syringae pv. aptata CFBP 1617 deposited in the PAMDB database; one strain was 100% homologous, and the other three were 99% homologous. To fulfill identification of the Serbian sugar beet isolates, gltA and rpoD partial gene sequences were determined (1), and the sequences were deposited as Accession Nos. KM386838 to KM386841 for gltA and KM386830 to KM38683033 for rpoD. The sequences were 100% homologous with those of pathotype strain CFBP 1617. Pathogenicity of each of four representative bacterial strains was tested on 3-week-old plants of the sugar beet cultivars Marinela, Serenada, and Jasmina (KWS, Belgrade, Serbia) and Lara (NS Seme, Novi Sad, Serbia) by atomizing a bacterial suspension of ~106 CFU/ml of the appropriate isolate onto the abaxial leaf surface of three plants per cultivar until water-soaking of the leaf surface was observed. Three plants of each cultivar atomized similarly with P. syringae pv. aptata CFBP 2473 and SDW served as positive and negative control treatments, respectively. Inoculated plants were kept in a clear plastic box at 80 to 100% RH and 17 ± 1°C and examined for symptom development over 3 weeks. For all test isolates and the control strain, inoculated leaves first developed water-soaked lesions 7 days after inoculation (DAI). By 10 to 14 DAI, lesions were necrotic and infection had spread to the petioles. By 21 DAI, wilting was observed on more than 50% of inoculated plants. Negative control plants were symptomless. Bacteria re-isolated onto NAS from inoculated leaves had the same colony morphology, LOPAT results, and gyrB partial gene sequences as described for the test strains. No bacteria were re-isolated from negative control plants. Based on these tests, the pathogen causing leaf spot on sugar beet in Serbia was identified as P. syringae pv. aptata. References: (1) P. Ferrente and M. Scortichini. Plant Pathol. 59:954, 2010. (2) R. A. Lelliott et al. J. Appl. Bacteriol. 29:470, 1966.

[Folic acid in the prevention of neural tube defects]. / Folna kiselina u prevenciji defekta neuralne cevi.

INTRODUCTION: The term neural tube defects (NTD) stands for anencephaly, iniencephaly, cephalocoele and spina-bifida. The cause of these anomalies is failure of brain spinal cord to properly develop, together with their protective shield of skull and spine, around the 4th gestational week. The prevalence of NTD in continental Europe is 11.2 10,000 live births. THE LEVEL OF FOLATES IN SERUM AND NTD: The level of folates in serum can influence the risk of a child affected with NTD. Studies on women with previous pregnancies with NTD showed that supplementary intake of folic acid, with or without other vitamins, preconceptual period throughout the first trimester has a preventive effect on its recurrence. Inadequate intake of folic acid is also connected with preterm delivery, intrauterine growth retardation and placental abruption and infarction. FOLATES IN NUTRITION: It is not folic acid, but folates, from the vitamin B group, that can naturally be found in food. There are several groups of folates that differ in the quantity by which they can be absorbed from food. Folates are temperature and storage sensitive and cooking can cause a significant fall of their concentration in food. FOLIC ACID SUPPLEMENTATION: The mean daily intake of folates by food is 0.218 mg whereas a reference nutritive intake for a woman of reproductive age is 0.2 mg per day. The currently recommended daily dose for prevention of first NTD occurrence is 0.4 mg, so it is clear that a certain amount of folic acid has to be supplemented preconceptionally and during the first trimester. It can be done in two ways, by telling all women to take it before conceiving, or to fortify food with sufficiently high doses of folic acid in order to achieve adequate serum levels. Neither of the ways is ideal, for not all women would take the supplement, and by aggressively fortifying the food, we create a potential hazard to those that do not need it and may have some problems with the excess of it. The best solution would be a widespread campaign about the need for folic acid and the risks of NTD. CONCLUSION: Recommendations of The Expert Advisory Group on Folic Acid in prevention of neural tube defects has several aspects (1) reducing the risk of the first NTD occurrence by preconceptional vitamin supplementation of folic acid in the dose of 0.4 mg day, which would go on until the end of the 12th week (2) reducing the risk of NTD recurrence in offspring of men and women with spina-bifida or with obstetric history affected with NTD by preconceptional vitamin supplementation of folic acid in the dose of 4 mg daily during the first 12 weeks and (3) organizing educational programmes for medical staff as well as the whole population in order to popularize vitamin supplementation.

[Inhibition of initial puerperal and postabortion lactation using oral prostaglandin E2 (Dinoprostone)]. / Inhibicija inicijalne puerperalne i postabortalne laktacije oralnom primenom prostaglandina E2 (dinoprostona).

Authors present their experience in oral administration of Prostaglandin E2 (Dinoproston, Upjohn) during postpartal and postabortal period (à 0.5 mg after legal pregnancy interruption) in suppression of lactation. Indications for postpartal lactation suppression were such as: stillbirth, postpartal neonatal death and maternal negative attitude towards breast feeding. The patients in whom the suppression of lactation was applied were of generative age (18-40 years) either primiparas or multiparas. All were delivered vaginally with no extra intrapartal or postpartal complications being the same in legal pregnancy interruptions which were performed by application of intravaginal, intracervical and intramuscular Prostaglandin preparations. The patients were administered 1 tbl od 0.5 mg Dinoproston preparation every 6-7 hours, 48 h after the delivery, i.e. 2 tbl in total (after meal). This method of lactation suppression was applied in 50 patients during 1990. Satisfactory results were achieved in all cases, while negative side effects and complications were not noted. Oral administration of PGE2 was found very efficient in postpartal and postabortal lactation suppression while compared with previously applied methods such as Estrogen-Testosterone preparation, i.e. small doses of Bromergon applied during 10-14 days. Oral administration of PG2 is more efficient and in a certain way more comfortable in relation to the previously applied methods.